Table 1.
Differential diagnosis of MOGAD associated-TM.
| Disorder | Multiple sclerosis | MOGAD | Aquaporin 4 positive NMOSD | Neurosarcoidosis | NeuroBehcet’s | Anti-GFAP astrocytopathy | Anti-CRMP-5 |
|---|---|---|---|---|---|---|---|
| Onset | Acute/subacute | Acute/subacute | Acute | Subacute/chronic | Acute/subacute | Acute/ subacute | Subacute |
| Evolution | Relapsing/progressive | Monophasic/relapsing | Relapsing | Progressive | Progressive | Progressive | Progressive |
| Clinical cues | Sensory symptoms predominantly. | Bladder/bowel symptoms. | Area postrema syndrome Other autoimmune comorbidities. (Ex SLE, Sjogren’s) |
Evidence of systemic involvement. (Ex: Lymphadenopathy) | History of recurrent oral or genital ulcers. | Associated with AQP4 ab and NMDA ab. Concomitant ovarian teratoma. |
History or increased risk for cancer. Constitutional symptoms. |
| Laboratory | |||||||
| Biomarkers | n/a | Anti-MOG ab in serum > > CSF | Aquaporin-4 ab in serum | n/a | N/A | Anti-GFAP ab in CSF > serum | Anti-CRPM5 ab in serum and CSF |
| CSF cells | Pleocytosis <50cells/μL (mainly lymphocytes) | Pleocytosis (mainly lymphocytes, neutrophils present in over 40%) | Pleocytosis (neutrophils predominant early on) | Pleocytosis (mainly lymphocytes) | Pleocytosis (neutrophils predominant) | Pleocytosis >50cells/μL (lymphocytes, monocytes) | Pleocytosis |
| O-bands unique to CSF | >80% | <10% | <20% | <20% | Rare | 50% | Can be present |
| Neuroimaging | |||||||
| Extension | Short/long if confluent lesions | LETM, short lesions may be present, conus medullaris involvement | LETM, up to 15% with short segment lesions | Short/LETM | Short/LETM | LETM | LETM |
| Number of lesions | Single/multifocal | Single or multifocal | Single | Single/multifocal | Single/multifocal | Single | Single |
| Location | Dorsal/lateral column | Central (30% only gray matter) H sign |
Central (gray and white matter) | Central / subpial/ leptomeningeal involvement | Central or anterior horn cells | Diffuse | Tract specific (lateral columns) |
| Enhancing | Nearly always in the acute setting | Enhancing in 50% cases acutely | Yes (most commonly in optic neuritis and transverse myelitis) Variable incidence of brain enhancing lesions |
Yes, usually persistent for months. | Yes | Often faint enhancement | Variable |
| Enhancing pattern | Ringlike or homogeneous | Faint; dorsal nerve root enhancement, cauda equina and pial enhancement may occur | Ringlike or patchy “cloud-like” Pencil-thin linear enhancement of the ependymal surface of lateral ventricles |
Dorsal subpial (trident sign) | Ringlike or non-specific (bagel sign) | Patchy, punctate and pia | Tract specific |
NA, not applicable; MOG, Myelin oligodendrocyte glycoprotein; MOGAD, Myelin oligodendrocyte glycoprotein antibody disease (MOGAD); ab, antibody; NMOSD, Neuromyelitis optica spectrum disorder; SLE, systemic lupus erythematosus; CSF, cerebrospinal fluid; GFAP, Glial fibrillary acidic protein; anti-CRPM-5, collapsin response-mediator protein-5; NMDA, N-methyl-D-aspartate; LETM, Longitudinal extensive transverse myelitis; O-bands, oligoclonal bands.